IF your younger relatives with the inherited tendency to thyroid dysfunction have a thyroid problem,it is likely an overactive gland.Usually the symptoms may incliude complaints you have had yourself such as nervousness,palpitations,shaky hands.On the other hand older relatives especially those over the age of fifty may have hypothyroidism with symptoms such as feeling cold,tired or lack of energy which they may just accept as signs of getting old.
manifestations of thyroid dysfunction vary considerably among relatives in their character and severity. Associated symptoms signs often progress slowly. Consequently, the accuracy of clinical diagnosis is limited.Your family physician must consider and exclude thyroid dysfunction much more often than they will establish a diagnosis. If only patients presenting with clearly suggestive symptoms and signs are evaluated, many affected family relatives will remain undiagnosed. For these persons, appropriate treatment for thyroid dysfunction or conservative monitoring to anticipate its potential future consequences can only be implemented when routine laboratory screening identifies them
A number of symptoms and signs are well-established manifestations of thyroid dysfunction. Additional findings in family histories indicate increased risk of developing thyroid dysfunction. Risk factors identifiable in family history include (1) previous thyroid dysfunction patient ; (2) goiter; (3) surgery or radiotherapy affecting the thyroid gland; (4) diabetes mellitus; (5) vitiligo; (6) pernicious anemia; (7) prematurely gray hair; and (8) medications and other compounds, such as lithium carbonate and iodine-containing compounds (eg, amiodarone hydrochloride, radiocontrast agents, expectorants containing potassium iodide, and kelp).
American Thyroid Association suggest The prevalences of various forms of thyroid dysfunction are substantial thus justifying population screening.
The prevalence of thyroid dysfunction in US adults is quite high:
Hypothyroidism 2%
Mild hypothyroidism 5-17%
Hyperthyroidism 0.2%
Mild hyperthyroidism 0.1-6.0%
The serum TSH assay is an accurate, widely available, safe, and relatively inexpensive diagnostic test for all common forms of hypothyroidism and hyperthyroidism.Screening of all newborn children for hypothyroidism is already a widely accepted and legislatively mandated practice.
In addition, serum TSH measurement in adults every 5 years has been shown by decision analysis to have equivalent or more favorable cost-effectiveness in comparison with other widely accepted disease detection strategies,for example, for hypertension, breast cancer, and hypercholesterolemia. The cost-effectiveness of screening is more favorable in women and older persons. Consequently,The American Thyroid Association recommends that adults be screened for thyroid dysfunction by measurement of the serum TSH concentration, beginning at age 35 years and every 5 years thereafter. Individuals with clinical manifestations potentially attributable to thyroid dysfunction and those with risk factors for its development may require more frequent serum TSH testing
MIMICS MENTAL ILLNESS
The psychiatric disturbances which accompany hyperthyroidism and hypothyroidism, the two commonest thyroid disorders, mimic mental illness. Family members with an overactive thyroid may exhibit marked anxiety and tension, emotional lability, impatience and irritability, distractible overactivity, exaggerated sensitivity to noise, and fluctuating depression with sadness and problems with sleep and the appetite. In extreme cases, they may appear schizophrenic, losing touch with reality and becoming delirious or hallucinating. An underactive thyroid can lead to progressive loss of interest and initiative, slowing of mental processes, poor memory for recent events, fading of the personality's colour and vivacity, general intellectual deterioration, depression with a paranoid flavour, and eventually, if not checked, to dementia and permanent harmful effects on the brain. In instances of each condition, some persons have been wrongly diagnosed, hospitalized for months, and treated unsuccessfully for psychosis.
Detection of the thyroid problem is complicated by the fact that more than one memeber of your family feels anxiety and tension to some degree, that many thyroid symptoms are similar to those of other diseases, and that hypothyroidism in particular often develops insidiously over a considerable time. But the results of overlooking the thyroid can be serious. It is very important for the physician to explore fully and give the tests for thyroid dysfunction, which today are relatively simple. When effective thyroid treatment is begun, the general response is quite favorable. Vitality returns and the mental processes become efficient again
THE DANGER STRESS CAN POSE FOR YOUR FAMILY
the relationship is clear between stress and the thyroid. The number of people who cite unusually stressful experiences before the onset of hyperthyroidism seems to bear out the theory of stress as a precipitating factor. While some members of your family can come through the same upheavals without developing thyroid disease, some perhaps are predisposed to it. On the other hand, it can be argued that the illness itself, before its symptoms are manifested, is contributing to the situation of stress.
RELATIONSHIP WITH PSYCHIATRIC CASES
Your family physician must also be careful to check the thyroid in cases where psychiatric medications must be taken over a long period. Lithium, the drug commonly used to stabilize the moods and increase the efficiency of manic-depressives, can cause hypothyroidism, particularly in middle-aged women who are the most susceptible to this trouble; the hypothyroidism in its turn can produce depression, the very problem that the treatment was intended to relieve.
HOW PREGNANT FAMILY MEMBERS ARE AFFECTED
Over the past decade there has been an increasing awareness that several disturbances of thyroid function may occur in mothers after delivery which may be more prevalent than previously appreciated. Also, patients with previous thyroid problems before pregnancy may have recurrences.In Osaka, Japan, a survey of mothers 3-8 months after delivery observed on overall incidence of thyroid dysfunction at 5.5% among 507.
In Uppsala, Sweden, the prevalence of biochemical post-partum thyroid dysfunction was 6.5% in a group of 460 women, representing an overall prevalence of 4.2% among the 644 women who entered the study
THE SYMPTOMS IN A NEW MOM
studies in Toronto over the last several years have demonstrated the prevalence of thyroid dysfunction and autoimmunity in testing mothers 6-24 weeks after delivery, have found a 7.1% incidence of abnormalities.The most common symptoms of post-partum(postnatal) hyperthyroidism occurring 6-12 weeks after delivery were fatigue, increased sweating, palpitations, and perhaps nervousness and weight loss; and subsequently, common symptoms occurring 12-24 weeks post-partum(postnatal) included fatigue, weight gain, lethargy and depression in the hypothyroid phase.
To determine most accurately the correct course of post-partum(poatnatal) hyperthyroidism, a thyroidal radioactive iodine uptake test is required in the hyperthyroid phase, while ceasing breast-feeding for several days
PLEASE KEEP YOUR COMMENTS,QUESTIONS AND SUGGESTIONS COMING.THEY ARE INVALUABLE TO THIS NOBLE EFFORT.THANK YOU FOR YOUR TIME
Thursday, August 7, 2008
WHAT YOU NEED TO KNOW ABOUT OOPHORITIS AS A WOMAN?
Oophoritis (ie, inflammation of the ovary) is an uncommonly used term for pelvic inflammatory disease (PID). This is an ascending infection of the ovaries and a major cause of female infectious morbidity(tisuue damage due to disease), ectopic pregnancy(conception elsewhere than in the uterus), and sterilization. Oophoritis is a clinically diagnosed disease that must be carefully distinguished from other causes of illness.
Infection ascends from bacterial colonization of the cervix and extends to the uterus, fallopian tubes, and ovaries. Gonorrhea and Chlamydia species(A sexually transmitted infection a.k.a cupid's itch) are typically colonized from the cervix in cases of oophoritis, but these pathogens are rarely isolated in ovarian tissue. These organisms instead facilitate infection of the adjoining anatomical parts like the uterus and the fallopian tubes by other bacteria. If left untreated, an abscess may form around the fallopian tubes and ovaries, a condition known as a tubo-ovarian abscess (TOA).
Frequency
United States
One million cases are reported each year.
International
Worldwide incidence and prevalence rates are unknown.
Mortality/Morbidity
In the United States, the Centers for Disease Control and Prevention (CDC) estimate that 150 women die each year and 100,000 women become infertile due to oophoritis. The other major morbidities are an increased risk of ectopic pregnancy and chronic pelvic pain.
Age
Oophoritis most commonly occurs in women younger than 25 years. When oophoritis occurs in postmenopausal women, it is usually associated with an underlying progressive and untreatable condition.
History
• Abdominal pain
• Pelvic pain
• Vaginal discharge
• Dyspareunia (painful intercourse)
• Fever
• Chills
• Nausea/vomiting
Physical
• Temperature greater than 38°C
• Abdominal tenderness in lower quadrants
• Possible rebound tenderness on pelvic examination
• Mucus/pus discharge
• Cervical motion tenderness
• Adnexal tenderness
• Adnexal mass (if a tubo-ovarian abscess is present)
Causes
• Unprotected sexual intercourse
• Multiple sexual partners
• High-risk sexual behavior
• Immunosuppression
• Recent instrumentation of genital tract (endometrial biopsy, intrauterine device [IUD] placement)
• Gynecologic malignancy (in postmenopausal women)
Medical Care
Outpatient treatment is appropriate for patients who are (1) hemodynamically stable(stil able to move around without aid), (2) sufficiently reliable to return for follow-up care, (3) immunocompetent, (4) not pregnant, (5) tolerant of oral medication, and (6) without clinical suspicion of a tubo-ovarian abscess (TOA).
Inpatient treatment is required for patients who (1) have already failed outpatient treatment, (2) are pregnant, (3) are infected with HIV or otherwise immunocompromised, (4) are exhibiting evidence of a TOA, (5) are hemodynamically unstable or appear septic, or (6) are unable to tolerate oral medications.
Surgical Care
Oophoritis may be managed with surgery when medical treatment fails to ameliorate symptoms after 48-72 hours. Surgical options may include laparoscopy(incision of the abdomen) with drainage of the abscess, removal of adnexa(adjoining tissues), and total abdominal hysterectomy(surgical of the uterus) oophorectomy (surgical removal of both ovaries)
Factors that influence the choice of surgery include extent of the abscess, degree of immunocompromise of the patient(damage to the immune system) , and preservation of fertility for future childbearing potential. Interventional radiology can sometimes be used for drainage of abscesses in patients who are not surgical candidates or in patients who prefer a less invasive procedure than surgery.
Consultations
If needed, consultation with obstetricians and gynecologists can be made for follow-up care and surgical expertise.
Diet
No changes are necessary. Nothing is to be taken orally if surgical treatment is anticipated.
Special Concerns
• Pregnancy
• Oophoritis in pregnancy is very uncommon.
• A consultation with an obstetrician/gynecologist is immediately required if this diagnosis is suspected.
• Pediatrics
• Children rarely have this condition.
• The provider must have a high suspicion for sexual abuse if PID is suspected in an adolescent patient.
Geriatrics: Elderly patients with PID are more likely to have an associated genital tract malignancy such as ovarian cancer or endometrial cancer.
PLEASE KEEP YOUR COMMENTS,QUESTIONS AND SUGGESTIONS COMING.THEY ARE INVALUABLE TO THIS NOBLE EFFORT.THANK YOU FOR YOUR TIME
Infection ascends from bacterial colonization of the cervix and extends to the uterus, fallopian tubes, and ovaries. Gonorrhea and Chlamydia species(A sexually transmitted infection a.k.a cupid's itch) are typically colonized from the cervix in cases of oophoritis, but these pathogens are rarely isolated in ovarian tissue. These organisms instead facilitate infection of the adjoining anatomical parts like the uterus and the fallopian tubes by other bacteria. If left untreated, an abscess may form around the fallopian tubes and ovaries, a condition known as a tubo-ovarian abscess (TOA).
Frequency
United States
One million cases are reported each year.
International
Worldwide incidence and prevalence rates are unknown.
Mortality/Morbidity
In the United States, the Centers for Disease Control and Prevention (CDC) estimate that 150 women die each year and 100,000 women become infertile due to oophoritis. The other major morbidities are an increased risk of ectopic pregnancy and chronic pelvic pain.
Age
Oophoritis most commonly occurs in women younger than 25 years. When oophoritis occurs in postmenopausal women, it is usually associated with an underlying progressive and untreatable condition.
History
• Abdominal pain
• Pelvic pain
• Vaginal discharge
• Dyspareunia (painful intercourse)
• Fever
• Chills
• Nausea/vomiting
Physical
• Temperature greater than 38°C
• Abdominal tenderness in lower quadrants
• Possible rebound tenderness on pelvic examination
• Mucus/pus discharge
• Cervical motion tenderness
• Adnexal tenderness
• Adnexal mass (if a tubo-ovarian abscess is present)
Causes
• Unprotected sexual intercourse
• Multiple sexual partners
• High-risk sexual behavior
• Immunosuppression
• Recent instrumentation of genital tract (endometrial biopsy, intrauterine device [IUD] placement)
• Gynecologic malignancy (in postmenopausal women)
Medical Care
Outpatient treatment is appropriate for patients who are (1) hemodynamically stable(stil able to move around without aid), (2) sufficiently reliable to return for follow-up care, (3) immunocompetent, (4) not pregnant, (5) tolerant of oral medication, and (6) without clinical suspicion of a tubo-ovarian abscess (TOA).
Inpatient treatment is required for patients who (1) have already failed outpatient treatment, (2) are pregnant, (3) are infected with HIV or otherwise immunocompromised, (4) are exhibiting evidence of a TOA, (5) are hemodynamically unstable or appear septic, or (6) are unable to tolerate oral medications.
Surgical Care
Oophoritis may be managed with surgery when medical treatment fails to ameliorate symptoms after 48-72 hours. Surgical options may include laparoscopy(incision of the abdomen) with drainage of the abscess, removal of adnexa(adjoining tissues), and total abdominal hysterectomy(surgical of the uterus) oophorectomy (surgical removal of both ovaries)
Factors that influence the choice of surgery include extent of the abscess, degree of immunocompromise of the patient(damage to the immune system) , and preservation of fertility for future childbearing potential. Interventional radiology can sometimes be used for drainage of abscesses in patients who are not surgical candidates or in patients who prefer a less invasive procedure than surgery.
Consultations
If needed, consultation with obstetricians and gynecologists can be made for follow-up care and surgical expertise.
Diet
No changes are necessary. Nothing is to be taken orally if surgical treatment is anticipated.
Special Concerns
• Pregnancy
• Oophoritis in pregnancy is very uncommon.
• A consultation with an obstetrician/gynecologist is immediately required if this diagnosis is suspected.
• Pediatrics
• Children rarely have this condition.
• The provider must have a high suspicion for sexual abuse if PID is suspected in an adolescent patient.
Geriatrics: Elderly patients with PID are more likely to have an associated genital tract malignancy such as ovarian cancer or endometrial cancer.
PLEASE KEEP YOUR COMMENTS,QUESTIONS AND SUGGESTIONS COMING.THEY ARE INVALUABLE TO THIS NOBLE EFFORT.THANK YOU FOR YOUR TIME
WHAT DOES YOUR FAMILY KNOW ABOUT ADDISON DISEASE?
WHAT DOES YOUR FAMILY KNOW ABOUT ADDISON DISEASE?
Hormone: chemical substance that is secreted at one point in the body and conveyed in the blood to regulate the normal body functions of tissues and organs elsewhere in the body.
Addison's disease occurs when the adrenal glands(ductless glands situated on the kidneys) do not produce enough of cortisol( hormone active in carbohydrate and protein metabolism) and, in some cases, the hormone aldosterone. The disease is referred to as adrenal insufficiency, or hypocortisolism. Causes of adrenal insufficiency can be grouped by the way in which they cause the adrenals to produce insufficient cortisol. These are adrenal dysgenesis (the gland has not formed adequately during development), impaired steroidogenesis (the gland is present but is biochemically unable to produce cortisol) or adrenal destruction (disease processes leading to the gland being damaged
Addison's disease is an endocrine or hormonal disorder that can afflict persons of any age, gender, or ethnicity, but it typically presents in adults between 30 and 50 years of age. Young women are most affected, outnumbering men by a factor of four
The disease is characterized by weight loss, muscle weakness, fatigue, low blood pressure, and sometimes darkening of the skin in both exposed and non-exposed parts of the body.
Cortisol
Cortisol is normally produced by the adrenal glands, located just above the kidneys. It belongs to a class of hormones called glucocorticoids, which affect almost every organ and tissue in the body. Scientists think that cortisol has possibly hundreds of effects in the body. Cortisol's most important job is to help the body respond to stress. Among its other vital tasks, cortisol
• helps maintain blood pressure and cardiovascular function(pertaining to the heart)
• helps slow the immune system damage
• helps balance the effects of insulin which regulates liver function
• helps regulate the metabolism of proteins, carbohydrates, and fats
• helps maintain proper arousal and sense of well-being
Because cortisol is so vital to health, the amount of cortisol produced by the adrenals is precisely balanced. Like many other hormones, cortisol is regulated by the brain and the pituitary gland, a bean-sized organ at the base of the brain. First, the hypothalamus sends "releasing hormones" to the pituitary gland. The pituitary responds by secreting hormones that regulate growth and thyroid and adrenal function, and sex hormones such as estrogen(A general term for female steroid sex hormones that are secreted by the ovary and responsible for typical female sexual characteristics) and testosterone( hormone produced chiefly by the testes; responsible for the development of male sex characteristics).
Aldosterone
Aldosterone produced by the adrenal glands. It helps maintain blood pressure and water and salt balance in the body. When aldosterone production falls too low, the kidneys are not able to regulate salt and water balance, causing blood volume and blood pressure to drop.
Causes
Failure to produce adequate levels of cortisol can occur for different reasons. The problem may be due to a disorder of the adrenal glands themselves (primary adrenal insufficiency) or to inadequate secretion of ACTH by the pituitary gland (secondary adrenal insufficiency).
Primary Adrenal Insufficiency
Addison's disease affects about 1 in 100,000 people. Most cases are caused by the gradual destruction of the adrenal cortex, the outer layer of the adrenal glands, by the body's own immune system. About 70 percent of reported cases of Addison's disease are caused by autoimmune disorders, in which the immune system makes antibodies that attack the body's own tissues or organs and slowly destroy them. Adrenal insufficiency occurs when at least 90 percent of the adrenal cortex has been destroyed. As a result, often both glucocorticoid (cortisol) and mineralocorticoid (aldostertone) hormones are lacking. Sometimes only the adrenal gland is affected; sometimes other glands also are affected, as in the polyendocrine deficiency syndrome.
Polyendocrine Deficiency Syndrome
The polyendocrine deficiency syndrome is classified into two separate forms, referred to as type I and type II.
Type I occurs in children, and adrenal insufficiency may be accompanied by
• slow sexual development
• pernicious anemia
• chronic Candida infections
• chronic active hepatitis
• hair loss (in very rare cases)
Type II, often called Schmidt's syndrome, usually afflicts young adults. Features of type II may include
• an underactive thyroid gland
• slow sexual development
• diabetes
• vitiligo
• loss of pigment on areas of the skin
Scientists think that the polyendocrine deficiency syndrome is inherited because frequently more than one family member tends to have one or more endocrine deficiencies.
Tuberculosis
Tuberculosis (TB), an infection which can destroy the adrenal glands, accounts for about 20 percent of cases of primary adrenal insufficiency in developed countries. When adrenal insufficiency was first identified by Dr. Thomas Addison in 1849, TB was found at autopsy in 70 to 90 percent of cases. As the treatment for TB improved, however, the incidence of adrenal insufficiency due to TB of the adrenal glands has greatly decreased.
Other Causes
Less common causes of primary adrenal insufficiency are
• chronic infection, mainly fungal infections
• cancer cells spreading from other parts of the body to the adrenal glands
• amyloidosis (often secondary to chronic rheumatoid arthritis)
• surgical removal of the adrenal glands
Secondary Adrenal Insufficiency
This form of adrenal insufficiency is much more common than primary adrenal insufficiency and can be traced to a lack of ACTH
Less commonly, adrenal insufficiency occurs when the pituitary gland either decreases in size or stops producing ACTH. These events can result from
• tumors or infections of the area
• loss of blood flow to the pituitary
• radiation for the treatment of pituitary tumors
• surgical removal of parts of the hypothalamus
• surgical removal of the pituitary gland
pituitary gland: The master gland of the endocrine system; located at the base of the brain
Symptoms
The symptoms of adrenal insufficiency usually begin gradually. Characteristics of the disease are
• chronic, worsening fatigue
• muscle weakness
• loss of appetite
• weight loss
About 50 percent of the time, one will notice
• nausea
• vomiting
• diarrhea
Other symptoms include
• low blood pressure that falls further when standing, causing dizziness or fainting
• skin changes in Addison's disease, with areas of dark tanning, covering exposed and non-exposed parts of the body; this darkening of the skin is most visible on scars; skin folds; pressure points such as the elbows, knees, knuckles, and toes; lips; and mucous membranes
Addison's disease can cause irritability and depression. Because of salt loss, a craving for salty foods also is common. In women, menstrual periods may become irregular or stop.
Because the symptoms progress slowly, they are usually ignored until a stressful event like an illness or an accident causes them to become worse. This is called an addisonian crisis, or acute adrenal insufficiency. In most cases, symptoms are severe enough that patients seek medical treatment before a crisis occurs. However, in about 25 percent of patients, symptoms first appear during an addisonian crisis.
Symptoms of an addisonian crisis include
• sudden penetrating pain in the lower back, abdomen, or legs
• severe vomiting and diarrhea
• dehydration
• low blood pressure
• loss of consciousness
Left untreated, an addisonian crisis can be fatal.
Diagnosis
In its early stages, adrenal insufficiency can be difficult to diagnose. A review of a patient's medical history based on the symptoms, especially the dark tanning of the skin, will lead a doctor to suspect Addison's disease.
A diagnosis of Addison's disease is made by laboratory tests. The aim of these tests is first to determine whether levels of cortisol are insufficient and then to establish the cause. X-ray exams of the adrenal and pituitary glands also are useful in helping to establish the cause.
ACTH Stimulation Test
This is the most specific test for diagnosing Addison's disease. In this test, blood cortisol, urine cortisol, or both are measured before and after a synthetic form of ACTH is given by injection. Patients with either form of adrenal insufficiency respond poorly or do not respond at all.
CRH Stimulation Test
When the response to the short ACTH test is abnormal, a "long" CRH stimulation test is required to determine the cause of adrenal insufficiency. Patients with primary adrenal insufficiency have high ACTHs. Patients with secondary adrenal insufficiency have absent or delayed ACTH responses.
Absent ACTH response points to the pituitary as the cause; a delayed ACTH response points to the hypothalamus as the cause.
Other Tests
Once a diagnosis of primary adrenal insufficiency has been made, x-ray exams of the abdomen may be taken to see if the adrenals have any signs of calcium deposits. Calcium deposits may indicate Tuberculosis. A tuberculin skin test also may be used.
If secondary adrenal insufficiency is the cause, doctors may use different imaging tools to reveal the size and shape of the pituitary gland. The most common is the CT scan The function of the pituitary and its ability to produce other hormones also are tested.
Treatment
Treatment of Addison's disease involves replacing, or substituting, the hormones that the adrenal glands are not making. Cortisol is replaced orally with tablets. If aldosterone is also deficient, it is replaced with oral doses.
Patients receiving aldosterone replacement therapy are usually advised by a doctor to increase their salt intake. Because patients with secondary adrenal insufficiency normally maintain aldosterone production, they do not require aldosterone replacement therapy. The doses of each of these medications are adjusted to meet the needs of individual patients.
During an addisonian crisis, low blood pressure, low blood glucose, and high levels of potassium can be life threatening. Standard therapy involves intravenous injections of hydrocortisone, saline (salt water), and dextrose (sugar). This treatment usually brings rapid improvement. When the patient can take fluids and medications by mouth, the amount of hydrocortisone is decreased until a maintenance dose is achieved
Special Problems
Surgery
Patients with chronic adrenal insufficiency who need surgery with general anesthesia are treated with injections of hydrocortisone and saline. Injections begin on the evening before surgery and continue until the patient is fully awake and able to take medication by mouth. The dosage is adjusted until the maintenance dosage given before surgery is reached.
Pregnancy
Women with primary adrenal insufficiency who become pregnant are treated with standard replacement therapy. If nausea and vomiting in early pregnancy interfere with oral medication, injections of the hormone may be necessary. During delivery, treatment is similar to that of patients needing surgery; following delivery, the dose is gradually tapered until after about 10 days.
Patient Education
A person who has adrenal insufficiency should always carry identification stating his or her condition in case of an emergency. The card should alert emergency personnel about the need to inject 100 mg of cortisol if its bearer is found severely injured or unable to answer questions. The card should also include the doctor's name and telephone number and the name and telephone number of the nearest relative to be notified. When traveling, a needle, syringe, and an injectable form of cortisol should be carried for emergencies. A person with Addison's disease also should know how to increase medication during periods of stress or mild upper respiratory infections. Immediate medical attention is needed when severe infections, vomiting, or diarrhea occur. These conditions can precipitate an addisonian crisis. A patient who is vomiting may require injections of hydrocortisone.
People with medical problems may wish to wear a descriptive warning bracelet or neck chain to alert emergency personnel. A number of companies manufacture medical identification products.
PLEASE KEEP YOUR COMMENTS,QUESTIONS AND SUGGESTIONS COMING.THEY ARE INVALUABLE TO THIS NOBLE EFFORT.THANK YOU FOR YOUR TIME
Hormone: chemical substance that is secreted at one point in the body and conveyed in the blood to regulate the normal body functions of tissues and organs elsewhere in the body.
Addison's disease occurs when the adrenal glands(ductless glands situated on the kidneys) do not produce enough of cortisol( hormone active in carbohydrate and protein metabolism) and, in some cases, the hormone aldosterone. The disease is referred to as adrenal insufficiency, or hypocortisolism. Causes of adrenal insufficiency can be grouped by the way in which they cause the adrenals to produce insufficient cortisol. These are adrenal dysgenesis (the gland has not formed adequately during development), impaired steroidogenesis (the gland is present but is biochemically unable to produce cortisol) or adrenal destruction (disease processes leading to the gland being damaged
Addison's disease is an endocrine or hormonal disorder that can afflict persons of any age, gender, or ethnicity, but it typically presents in adults between 30 and 50 years of age. Young women are most affected, outnumbering men by a factor of four
The disease is characterized by weight loss, muscle weakness, fatigue, low blood pressure, and sometimes darkening of the skin in both exposed and non-exposed parts of the body.
Cortisol
Cortisol is normally produced by the adrenal glands, located just above the kidneys. It belongs to a class of hormones called glucocorticoids, which affect almost every organ and tissue in the body. Scientists think that cortisol has possibly hundreds of effects in the body. Cortisol's most important job is to help the body respond to stress. Among its other vital tasks, cortisol
• helps maintain blood pressure and cardiovascular function(pertaining to the heart)
• helps slow the immune system damage
• helps balance the effects of insulin which regulates liver function
• helps regulate the metabolism of proteins, carbohydrates, and fats
• helps maintain proper arousal and sense of well-being
Because cortisol is so vital to health, the amount of cortisol produced by the adrenals is precisely balanced. Like many other hormones, cortisol is regulated by the brain and the pituitary gland, a bean-sized organ at the base of the brain. First, the hypothalamus sends "releasing hormones" to the pituitary gland. The pituitary responds by secreting hormones that regulate growth and thyroid and adrenal function, and sex hormones such as estrogen(A general term for female steroid sex hormones that are secreted by the ovary and responsible for typical female sexual characteristics) and testosterone( hormone produced chiefly by the testes; responsible for the development of male sex characteristics).
Aldosterone
Aldosterone produced by the adrenal glands. It helps maintain blood pressure and water and salt balance in the body. When aldosterone production falls too low, the kidneys are not able to regulate salt and water balance, causing blood volume and blood pressure to drop.
Causes
Failure to produce adequate levels of cortisol can occur for different reasons. The problem may be due to a disorder of the adrenal glands themselves (primary adrenal insufficiency) or to inadequate secretion of ACTH by the pituitary gland (secondary adrenal insufficiency).
Primary Adrenal Insufficiency
Addison's disease affects about 1 in 100,000 people. Most cases are caused by the gradual destruction of the adrenal cortex, the outer layer of the adrenal glands, by the body's own immune system. About 70 percent of reported cases of Addison's disease are caused by autoimmune disorders, in which the immune system makes antibodies that attack the body's own tissues or organs and slowly destroy them. Adrenal insufficiency occurs when at least 90 percent of the adrenal cortex has been destroyed. As a result, often both glucocorticoid (cortisol) and mineralocorticoid (aldostertone) hormones are lacking. Sometimes only the adrenal gland is affected; sometimes other glands also are affected, as in the polyendocrine deficiency syndrome.
Polyendocrine Deficiency Syndrome
The polyendocrine deficiency syndrome is classified into two separate forms, referred to as type I and type II.
Type I occurs in children, and adrenal insufficiency may be accompanied by
• slow sexual development
• pernicious anemia
• chronic Candida infections
• chronic active hepatitis
• hair loss (in very rare cases)
Type II, often called Schmidt's syndrome, usually afflicts young adults. Features of type II may include
• an underactive thyroid gland
• slow sexual development
• diabetes
• vitiligo
• loss of pigment on areas of the skin
Scientists think that the polyendocrine deficiency syndrome is inherited because frequently more than one family member tends to have one or more endocrine deficiencies.
Tuberculosis
Tuberculosis (TB), an infection which can destroy the adrenal glands, accounts for about 20 percent of cases of primary adrenal insufficiency in developed countries. When adrenal insufficiency was first identified by Dr. Thomas Addison in 1849, TB was found at autopsy in 70 to 90 percent of cases. As the treatment for TB improved, however, the incidence of adrenal insufficiency due to TB of the adrenal glands has greatly decreased.
Other Causes
Less common causes of primary adrenal insufficiency are
• chronic infection, mainly fungal infections
• cancer cells spreading from other parts of the body to the adrenal glands
• amyloidosis (often secondary to chronic rheumatoid arthritis)
• surgical removal of the adrenal glands
Secondary Adrenal Insufficiency
This form of adrenal insufficiency is much more common than primary adrenal insufficiency and can be traced to a lack of ACTH
Less commonly, adrenal insufficiency occurs when the pituitary gland either decreases in size or stops producing ACTH. These events can result from
• tumors or infections of the area
• loss of blood flow to the pituitary
• radiation for the treatment of pituitary tumors
• surgical removal of parts of the hypothalamus
• surgical removal of the pituitary gland
pituitary gland: The master gland of the endocrine system; located at the base of the brain
Symptoms
The symptoms of adrenal insufficiency usually begin gradually. Characteristics of the disease are
• chronic, worsening fatigue
• muscle weakness
• loss of appetite
• weight loss
About 50 percent of the time, one will notice
• nausea
• vomiting
• diarrhea
Other symptoms include
• low blood pressure that falls further when standing, causing dizziness or fainting
• skin changes in Addison's disease, with areas of dark tanning, covering exposed and non-exposed parts of the body; this darkening of the skin is most visible on scars; skin folds; pressure points such as the elbows, knees, knuckles, and toes; lips; and mucous membranes
Addison's disease can cause irritability and depression. Because of salt loss, a craving for salty foods also is common. In women, menstrual periods may become irregular or stop.
Because the symptoms progress slowly, they are usually ignored until a stressful event like an illness or an accident causes them to become worse. This is called an addisonian crisis, or acute adrenal insufficiency. In most cases, symptoms are severe enough that patients seek medical treatment before a crisis occurs. However, in about 25 percent of patients, symptoms first appear during an addisonian crisis.
Symptoms of an addisonian crisis include
• sudden penetrating pain in the lower back, abdomen, or legs
• severe vomiting and diarrhea
• dehydration
• low blood pressure
• loss of consciousness
Left untreated, an addisonian crisis can be fatal.
Diagnosis
In its early stages, adrenal insufficiency can be difficult to diagnose. A review of a patient's medical history based on the symptoms, especially the dark tanning of the skin, will lead a doctor to suspect Addison's disease.
A diagnosis of Addison's disease is made by laboratory tests. The aim of these tests is first to determine whether levels of cortisol are insufficient and then to establish the cause. X-ray exams of the adrenal and pituitary glands also are useful in helping to establish the cause.
ACTH Stimulation Test
This is the most specific test for diagnosing Addison's disease. In this test, blood cortisol, urine cortisol, or both are measured before and after a synthetic form of ACTH is given by injection. Patients with either form of adrenal insufficiency respond poorly or do not respond at all.
CRH Stimulation Test
When the response to the short ACTH test is abnormal, a "long" CRH stimulation test is required to determine the cause of adrenal insufficiency. Patients with primary adrenal insufficiency have high ACTHs. Patients with secondary adrenal insufficiency have absent or delayed ACTH responses.
Absent ACTH response points to the pituitary as the cause; a delayed ACTH response points to the hypothalamus as the cause.
Other Tests
Once a diagnosis of primary adrenal insufficiency has been made, x-ray exams of the abdomen may be taken to see if the adrenals have any signs of calcium deposits. Calcium deposits may indicate Tuberculosis. A tuberculin skin test also may be used.
If secondary adrenal insufficiency is the cause, doctors may use different imaging tools to reveal the size and shape of the pituitary gland. The most common is the CT scan The function of the pituitary and its ability to produce other hormones also are tested.
Treatment
Treatment of Addison's disease involves replacing, or substituting, the hormones that the adrenal glands are not making. Cortisol is replaced orally with tablets. If aldosterone is also deficient, it is replaced with oral doses.
Patients receiving aldosterone replacement therapy are usually advised by a doctor to increase their salt intake. Because patients with secondary adrenal insufficiency normally maintain aldosterone production, they do not require aldosterone replacement therapy. The doses of each of these medications are adjusted to meet the needs of individual patients.
During an addisonian crisis, low blood pressure, low blood glucose, and high levels of potassium can be life threatening. Standard therapy involves intravenous injections of hydrocortisone, saline (salt water), and dextrose (sugar). This treatment usually brings rapid improvement. When the patient can take fluids and medications by mouth, the amount of hydrocortisone is decreased until a maintenance dose is achieved
Special Problems
Surgery
Patients with chronic adrenal insufficiency who need surgery with general anesthesia are treated with injections of hydrocortisone and saline. Injections begin on the evening before surgery and continue until the patient is fully awake and able to take medication by mouth. The dosage is adjusted until the maintenance dosage given before surgery is reached.
Pregnancy
Women with primary adrenal insufficiency who become pregnant are treated with standard replacement therapy. If nausea and vomiting in early pregnancy interfere with oral medication, injections of the hormone may be necessary. During delivery, treatment is similar to that of patients needing surgery; following delivery, the dose is gradually tapered until after about 10 days.
Patient Education
A person who has adrenal insufficiency should always carry identification stating his or her condition in case of an emergency. The card should alert emergency personnel about the need to inject 100 mg of cortisol if its bearer is found severely injured or unable to answer questions. The card should also include the doctor's name and telephone number and the name and telephone number of the nearest relative to be notified. When traveling, a needle, syringe, and an injectable form of cortisol should be carried for emergencies. A person with Addison's disease also should know how to increase medication during periods of stress or mild upper respiratory infections. Immediate medical attention is needed when severe infections, vomiting, or diarrhea occur. These conditions can precipitate an addisonian crisis. A patient who is vomiting may require injections of hydrocortisone.
People with medical problems may wish to wear a descriptive warning bracelet or neck chain to alert emergency personnel. A number of companies manufacture medical identification products.
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